IFN- alpha blocks IL-17 production by peripheral blood mononuclear cells in patients with chronic active hepatitis B Infection
1 Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, Yuzhong District, China
2 Department of Obstetrics and Gynecology, Assisited Reproductive Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
BMC Infectious Diseases 2014, 14:55 doi:10.1186/1471-2334-14-55Published: 1 February 2014
IFN-α has been used to treat patients with chronic active hepatitis B (CAHB). Recent studies have implicated the IL-23/Th-17 pathway in the pathogenesis of CAHB. In this study, we investigated whether IFN-α could affect this pathway.
Peripheral blood mononuclear cells (PBMCs) obtained from patients with active CAHB (n = 61) and controls (n = 32) were cultured with or without IFN-α, and the levels of IL-17 and IL-10 in the supernatants were determined by ELISA, while the frequency of IL-17-expressing cells was measured by FACS. Similar experiments were also conducted with isolated CD4+ T cells from controls. Furthermore, an experiment using an anti-IL-10 antibody was performed to examine the underlying mechanisms of action of IFN-α.
Both the levels of IL-17 and the frequency of IL-17-expressing cells were significantly higher in the PBMCs from CAHB patients than in the controls. IFN-α significantly decreased IL-17 production and the frequency of IL-17-expressing cells in PBMCs from both patients and controls. On the other hand, IFN-α increased IL-10 production by PBMCs from patients and controls. Anti-IL-10 antibody was able to neutralize the inhibitory effect of IFN-α on IL-17 production by PBMCs.
In vitro experiments showed that IFN-α could inhibit IL-17 expression and increase IL-10 production by PBMCs and CD4+ T cells. The inhibitory role of IFN-α on IL-17 production was partly mediated by IL-10.